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Responses to our 15 Questions: part 2

Questions 4–8

Responses to our 15 Questions: part 2

Responses to our 15 Questions: part 1

Here we continue our appraisal of various attempts to answer our 15 Questions for Evolutionists. We’ve compiled many of the answers that we’ve received to date (paraphrased to cover as many versions of the answer we’ve received as possible), along with our refutations.

4. Why is natural selection, a principle recognized by creationists, taught as ‘evolution’, as if it explains the origin of the diversity of life?

Demonstrating some example of natural selection is not demonstrating ‘evolution in action’ because no new genetic specifications are being created by natural selection.

Answer 1: It is disingenuous for creationists to claim to accept natural selection and not ‘macroevolution’, since the cumulative effect of the former leads to the latter.

Rebuttal: Actually, there is not one undisputed example of one structure arising gradually through natural selection. But if natural selection was the engine for evolution, we should have many examples of this happening. Rather, every example of natural selection that we have shows that it is a conservative force which specializes creatures to be better adapted for their environment. This involves a loss of information; for example, a population of bears in a cold climate losing information for short and medium-length fur (see How information is lost when creatures adapt to their environment).

The major issue here is that natural selection does not create any genetic information, so ‘natural selection’ is not the same as evolution. Demonstrating some example of natural selection is not demonstrating ‘evolution in action’ because no new genetic specifications are being created by natural selection. So there is nothing disingenuous about creationists accepting natural selection but not molecules-to-molecular-biologists evolution. However, it is disingenuous of evolutionists to continually equate natural selection with evolution.

However, high-profile evolutionists themselves have long recognized that ‘macroevolution’ is not just a matter of more ‘microevolution’; it is qualitatively different (so CMI advises against using these terms, which tend to create confusion). In November 1980 a conference of some of the world’s leading evolutionary biologists, billed as ‘historic’, was held at the Chicago Field Museum of Natural History on the topic of ‘macroevolution’. Reporting on the conference in the journal Science (Vol. 210(4472):883–887, 1980.), Roger Lewin wrote:

“The central question of the Chicago conference was whether the mechanisms underlying microevolution can be extrapolated to explain the phenomena of macroevolution. At the risk of doing violence to the positions of some of the people at the meeting, the answer can be given as a clear, No.”

Francisco Ayala (Associate Professor of Genetics, University of California), was quoted in the same article as saying:

“… but I am now convinced from what the paleontologists say that small changes do not accumulate.”
Answer 2: There are over 100 new mutations for every child born. It is inevitable that evolution would happen with this rate of mutation. Those with the best mutations survive and reproduce.

Rebuttal: We’ve noted the mutation rate—and that it’s a huge problem for evolution. 100 mutations is actually the lowest (unrealistically low) possible number of new mutations per person, and that’s already extremely problematic for evolution.

When a person reproduces, his genes as a whole (half of them) are passed on, with both beneficial and non-beneficial mutations. It’s not as if a certain gene gets selected—it’s the group of genes that the person has. Most mutations are nearly neutral, emphasis on nearly. We don’t need to worry about the really catastrophic mutations being passed on most of the time; they often result in the death of the individual or otherwise prevent reproduction (natural selection operates here to remove the lethal ones, thus acting as a conserving force).

But most mutations aren’t like that—the person can survive. The deleterious effect may be so small that it’s imperceptible by itself. But add up thousands, hundreds of thousands, of those mutations, and you have a substantially ‘less fit’ individual than someone from the first generation. This person isn’t an example of evolution—he’s an example of devolution. He’s more likely to have problems like allergies and immune system disorders, he’s more likely to have trouble reproducing, and he’s probably got a shorter lifespan (without modern medical help), just for starters. And it gets worse for his descendants, because eventually all these mutations build up to an unsustainable level, and we get a situation that Dr John Sanford, geneticist, describes in Genetic Entropy and the Mystery of the Genome (see our review):

“When selection is unable to counter the loss of information due to mutations, a situation arises called ‘error catastrophe’. If not rapidly corrected, this situation leads to the eventual death of the species—extinction! In its final stages, genomic degeneration leads to declining fertility, which curtails further selection (selection always requires a surplus population, some of which can then be eliminated each generation). Inbreeding and genetic drift then take over entirely, rapidly finishing off the population. The process is an irreversible downward spiral. This advanced stage of genomic degeneration is called ‘mutational meltdown’. Mutational meltdown is recognized as an immediate threat to all of today’s endangered species. The same process appears to potentially be a theoretical threat for mankind” (p. 41).

5. How did new biochemical pathways, which involve multiple enzymes working together in sequence, originate?

Answer 1: There’s no reason to think that the first life was as complex as today’s—the simplest forms would be extinct by now, out-competed by the more complex modern forms. A self-replicator can be as simple as a strand of six DNA nucleotides. These self-replicators set the stage for evolution to begin whether or not you call these molecules ‘life’.

Rebuttal: Documentation? Evidence? Hard science indicates that the simplest life is incredibly complex (we have already cited How simple can life be?). So your imaginary scenario is just that; far removed from what we know of life on Earth. For more on claims of self-replicating molecules, peptides and enzymes, see Self-replicating enzymes? A critique of some current evolutionary origin-of-life models.

Answer 2: Furthermore, looking at the biochemical processes in detail at a moment in time does not indicate the evolutionary history of an organism. Scaffolding is a means to develop a process. Furthermore, evolution is established on the macroscopic level through morphology as well as on the molecular level with genetics. As the understanding of biochemistry proceeds (as it is a much younger science), a better understanding will develop. Furthermore, as Michael Behe learned at the Dover trial, there is a lot known about the evolution of proteins, such as with the immune system.

Rebuttal: Lots of assertions here with little to back them up. Taking each sentence in turn:

In one sense, it is good to see that some evolutionists have finally abandoned the discredited “ontogeny recapitulates phylogeny”argument applied to biochemistry. But this also exposes the inconsistency of a major evolutionary argument: supposedly the many biochemical similarities prove evolution from a common ancestor with these features. But then it turns out that the ancestor didn’t have these features at all! E.g., all life uses DNA because of common ancestry, but then this common ancestor didn’t use DNA. Or, there is a common pentadactyl (five-digit) limb pattern in all tetrapods, because they all came from a common ancestor that walked up on the land from the sea. But the usual candidates for this common ancestor don’t have five digits—Acanthostega had eight, while Ichthyostega had seven, although all of these, including the much hyped Tiktaalik, have been trumped by more recent fossil evidence.

Scaffolding is really the “spandrel” argument by Lewontin and Gould.1 Yet there is no further evidence presented.

The morphological evidence is dealt with elsewhere, and is a change of subject.

There is yet another quasi-prophetic appeal to what we will understand in the future, but this is of course a tacit admission that evolutionists don’t have an answer now.

Lots of rubbish has been talked about the Dover Trial, where a previously unknown judge became the darling of the liberal media and evolution-pushing organizations by parroting the ACLU submission in his verdict. See our analysis.

Answer 3: It’s not a lucky accident!

Rebuttal: And if the question was, “Was the origination of new biochemical pathways, which involve multiple enzymes working together in a sequence, a lucky accident?”, that would be an answer to our question, although still only an unsupported assertion. Either it’s a lucky accident or it’s designed. Selection can’t work before these already exist in a functional form—it’s pure chance. But the question was how did they come about, and this didn’t even attempt to answer that one.

6. Living things look like they were designed, so how do evolutionists know that they were not designed?

Answer 1: They don’t, but to say they are is a mere argument from ignorance.

Rebuttal: If evolutionists admit they don’t know, isn’t that by definition an admission that they’re arguing from ignorance? Also, as stated in part 1, the argument from design is based on what we do know.

Answer 2: If there were a designer, we should see designs tending toward simplicity, not complexity. Yet that is the opposite of what we see.

Rebuttal: So life is too complex for it to be designed? This is a new one! In any case, this is only a form of argument from bad design, refuted in a number of articles under What about claims of ‘bad design’?

Actually, the critic also forgets the Fall, so we should see degeneration, as pointed out in our book By Design. We have previously noted that many parasites are genetically depleted compared to free-living equivalents—see articles under How does biblical Christianity explain the origin of poisons, and pathogenic bacteria and viruses. Thus it should be called devolution not evolution (a downhill change is consistent with the biblical Creation-Fall model). This was backed up by an interview with famous evolutionist Lynn Margulis in Discover April 2011:

“Both the treponema that cause syphilis and the borrelia that cause Lyme disease contain only a fifth of the genes they need to live on their own. Related spirochetes that can live outside by themselves need 5,000 genes, whereas the spirochetes of those two diseases have only 1,000 genes in their bodies. The 4,000 missing gene products needed for bacterial growth can be supplied by wet, warm human tissue. This is why both the Lyme disease borrelia and syphilis treponema are symbionts—they require another body to survive.”

Answer 3: Vestigial organs provide evidence of evolution: these are structures which once had a purpose but no longer do.

Rebuttal: 100 years ago, there were dozens of organs and systems were thought to be vestigial. Today, we know of uses for every organ on those lists. In some cases, an organ serves no essential or known function in the adult, but in the developing stages it serves a critical role. See a few examples under Performing surgery upon evolutionary thinking (interview with pediatric surgeon Dr Ross Pettigrew).

Just because we don’t know of a function for a certain organ or system doesn’t mean there is none.

Furthermore, it’s ironic that this critic accused us of using an “argument from ignorance”, then did just that! Just because we don’t know of a function for a certain organ or system doesn’t mean there is none. One important and recently discovered function of the appendix—a safe house for beneficial bacteria—should have been a lesson. At least, that should have been the argument 100 years ago. Today, we know better. See also Do any vestigial organs exist in humans?.

Answer 4: There are structures that would be horrendously designed, but they’re easy to explain if they evolved. The laryngeal nerve is one example of this.

Rebuttal: See our article on the laryngeal nerve.

Answer 5: It’s very lucky that everything works out just so it looks like it were designed, but if it weren’t, we wouldn’t be around to notice it.

Rebuttal: It’s a simple explanation—except it’s not an explanation. The analogy that we have borrowed to show the inadequacy of the explanation is if I were surrounded by an execution squad comprising expert marksmen, each person with a rifle, and they all fired, but I was still alive afterwards, it’s equally true that if it hadn’t happened that way I wouldn’t be around to observe it, but that doesn’t mean I shouldn’t be surprised by it. So that we exist doesn’t make it any less surprising that we do.

7. How did multi-cellular life originate?

Answer 1: It was beneficial for cells to work together.

Rebuttal: That may be true, but while that may tell us why such a fully developed system is advantageous, it says nothing about how such a system originated, and what benefits the incomplete stages would have.

Answer 2: Colonies of cells that cooperated were the first step.

Rebuttal: There is a huge difference between a colony of single-celled organisms and a true multi-celled organism, and no known mechanism would enable an organism to make that leap. For example, there is a big jump between selection for single cell reproductive success and that for integrity of a multicellular organism. In complex creatures, great reproductive success of a single cell type is usually called cancer. See Evolution of muticellularity: what is required?

8. How did sex originate?

Answer 1: Sexual reproduction allows for evolution at a much faster pace than asexual reproduction. Organisms that exchanged DNA were thus able to evolve out of situations that might have killed their asexual counterparts.

Rebuttal: Another answer which tells why but not how. Creationists can explain the origin of fully functioning sexual reproduction, from the start, in an optimal and genetically diverse population, at the hand of an intelligent Creator. Once the mechanisms are already in place, they have these advantages. But simply having advantages doesn’t remotely explain how they could be built from scratch. The hypothetical transitional forms would be highly disadvantageous, so natural selection would work against them. Sexual reproduction involves fine tuning on both the molecular level (so DNA from two individuals can combine into a new one) and the macroscopic level: in many cases, the male and female genitalia are precisely tuned so one could fit the other, meaning that they could not have evolved independently.

It’s also only partially right: yes, because of recombination, sexual reproduction allows much variability. But it also allows a successful organism to pass on only half the genes to any given offspring (and in a stable population by definition, there is only one offspring per parent). This acts as a conservative force. This is a good thing, because most mutations are harmful, and it’s a good thing they are not passed on. But for evolution, it’s a problem since any putatively beneficial mutation has a 50% chance of not being passed on. Also, sexual reproduction allows these harmful genes, if recessive, to be shielded by a backup copy.

Answer 2: Sex depends on both the male and the female. Any incompatibilities would cause sterility and would be selected against.

Rebuttal: Sex is indeed dependent on the actions of the male and the female, but unless you’re some kind of neo-Lamarckian, that isn’t going to lead to complementary structures. The fact that natural selection will weed out sterile individuals doesn’t explain how functioning sexual reproduction came to be, since there’s a lot more ways to make something that doesn’t work than something that does. Incidentally, many responses to this question show more confidence about the origin of sex than Dawkins had. See Evolution of Sex (Refuting Evolution 2 chapter 11).

Published: 14 September 2011


  1. See Gould, S.J. and Lewontin, R.C., The spandrels of San Marco and the Panglossian Paradigm: a critique of the adaptationist programme, Proceedings of the Royal Society of London, Series B, 205(1161):581–598, 1979. Return to text.

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